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Potassium ATP channel function is altered in mesenteric arteries of old high salt fed rats
Author(s) -
Whidden Melissa Ann,
Basgut Bilgen,
Kirichenko Nataliya,
Erdos Benedek,
Tumer Nihal
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.860.10
Subject(s) - cromakalim , mesenteric arteries , glibenclamide , medicine , endocrinology , vasodilation , dilator , acetylcholine , contraction (grammar) , chemistry , artery , diabetes mellitus
Hypertension is a risk factor for cardiovascular disease and dietary salt is a contributing factor to high blood pressure. Increased salt intake in the elderly has been shown to impair relaxation of resistance vessels. Therefore, we examined whether a high salt (HS) diet alters the function of K ATP channels in mesenteric arteries (MAs) from young and old rats. Young (7 mo) and old (29 mo) F‐344xBN rats were fed a control or HS diet (8% NaCl) for 12 days and 2 nd order MAs were used for vascular measurements. Acetylcholine (Ach)‐induced relaxation was significantly reduced with age. Relaxation to Ach was 92 ± 2% in young vs. 81 ± 4% in old arteries. Pretreatment with the K ATP channel blocker glibenclamide only reduced relaxation to Ach in young MAs. On a HS diet, dilation to Ach was reduced in old salt MAs (60 ± 3%) when compared with old control arteries (81 ± 4%; P<0.001). Glibenclamide reduced Ach‐induced dilation in young salt MAs but had no effect on old salt MAs. Cromakalim (K ATP channel opener) dilation was reduced in old salt MAs when compared with old control arteries. Maximal relaxation to cromakalim was 99 ± 1% in old control vs. 85 ± 5% in old salt arteries (P<0.05). These findings demonstrate that age impairs endothelium‐dependent dilation in MAs. Furthermore, a HS diet alters the function of K ATP channels in isolated MAs and affects the mediation of dilator stimuli. Supported by the Medical Research Service of the Department of Veterans Affairs and NIA T32 AG000196 award.